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Crossroads between light response and nutrient signalling: ENV1 and PhLP1 act as mutual regulatory pair in
Doris Tisch, Andre Schuster, Monika Schmoll1
1AIT Austrian Institute of Technology, Department Health and Environment, Bioresources, Konrad Lorenz Strasse 24, 3430 Tulln, Austria. monika.schmoll@ait.ac.at.
Background:
Crosstalk between the signalling pathways responding to light-dark cycles and those triggering the adaptation of metabolism to the environment is known to occur in various organisms. This interrelationship of light response and nutrient sigalling is crucial for health and fitness. The tropical ascomycete Trichoderma reesei (syn. Hypocrea jecorina) represents one of the most efficient plant cell wall degraders. Regulation of the enzymes required for this process is affected by nutritional signals as well as other environmental signals including light. Therefore we aimed to elucidate the interrelationship between nutrient and light signaling and how the light signal is transmitted to downstream pathways.
Results:
We found that the targets of the light regulatory protein ENV1 in light show considerable overlap with those of the heterotrimeric G-protein components PhLP1, GNB1 and GNG1. Detailed investigation of a regulatory interrelationship of these components with ENV1 under conditions of early and late light response indicated a transcriptional mutual regulation between PhLP1 and ENV1, which appears to dampen nutrient signalling during early light response, presumably to free resources for protective measures prior to adaptation of metabolism to light. Investigating the downstream part of the cascade we found support for the hypothesis that ENV1 is necessary for cAMP mediated regulation of a considerable part of the core functions of the output pathway of this cascade, including regulation of glycoside hydrolase genes and those involved in nitrogen, sulphur and amino acid metabolism.
Conclusions:
ENV1 and PhLP1 are mutual regulators connecting light signaling with nutrient signaling, with ENV1 triggering the output pathway by influencing cAMP levels.
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